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Cruickshanks KJ, Klein R, Klein BEK, Wiley TL, Nondahl DM, Tweed TS. Cigarette Smoking and Hearing Loss: The Epidemiology of Hearing Loss Study. JAMA. 1998;279(21):1715–1719. doi:10.1001/jama.279.21.1715
From the Department of Ophthalmology and Visual Sciences (Drs Cruickshanks, R. Klein, and B. E. K. Klein and Messrs Nondahl and Tweed) and the Department of Communicative Disorders (Dr Wiley and Mr Tweed), University of Wisconsin, Madison.
Context.— Clinical studies have suggested that cigarette smoking may be associated
with hearing loss, a common condition affecting older adults.
Objective.— To evaluate the association between smoking and hearing loss.
Design.— Population-based, cross-sectional study.
Setting.— Community of Beaver Dam, Wis.
Participants.— Adults aged 48 to 92 years. Of 4541 eligible subjects, 3753 (83%) participated
in the hearing study.
Main Outcome Measures.— The examination included otoscopy, screening tympanometry, and pure-tone
air-conduction and bone-conduction audiometry. Smoking history was ascertained
by self-report. Hearing loss was defined as a pure-tone average (0.5, 1, 2,
and 4 kHz) greater than 25-dB hearing level in the worse ear.
Results.— After adjusting for other factors, current smokers were 1.69 times as
likely to have a hearing loss as nonsmokers (95% confidence interval, 1.31-2.17).
This relationship remained for those without a history of occupational noise
exposure and in analyses excluding those with non–age-related hearing
loss. There was weak evidence of a dose-response effect. Nonsmoking participants
who lived with a smoker were more likely to have a hearing loss than those
who were not exposed to a household member who smoked (odds ratio, 1.94; 95%
confidence interval, 1.01-3.74).
Conclusions.— These data suggest that environmental exposures may play a role in age-related
hearing loss. If longitudinal studies confirm these findings, modification
of smoking habits may prevent or delay age-related declines in hearing sensitivity.
HEARING LOSS is estimated to affect 30% to 35% of adults aged 65 to
75 years in the United States, yet little is known about the etiology of this
disorder.1 Whereas hearing loss may be an inevitable
consequence of aging, representing the cumulative damage from products of
normal cellular metabolic processes, some studies of rural African tribes
have failed to find a decline in hearing sensitivity with age.2,3
This may suggest that genetic, environmental, and lifestyle factors play a
role in the development of presbycusis, age-related hearing loss.
Cigarette smoking may affect hearing through its effects on antioxidative
mechanisms or on the vasculature supplying the auditory system.4,5
An association between cigarette smoking and hearing loss among adults has
been found in some clinical studies.6-9
Weiss7 found that men who smoked more than
1 pack per day had worse hearing thresholds at 250 to 1000 Hz than nonsmokers
or "light" smokers, but there was no difference at higher frequencies. Siegelaub
et al9 reported on a large study of 33146 men
and women seen at Kaiser-Permanente, Oakland, Calif. Among men without a history
of noise exposure, current smokers were more likely than nonsmokers to have
a hearing loss at 4000 Hz, but the size of the effect was small. There was
no association among women. The Baltimore Longitudinal Study of Aging10 found no association between cigarette smoking and
the development of a hearing loss in 531 white, upper-middle-class men.
There have been few population-based studies of smoking and hearing.
In the Health Interview Survey,11 men who smoked
2 or more packs per day were more likely to report having a hearing loss than
nonsmokers. In the Framingham Study,12 which
tested hearing with audiometry, there was no association between cigarette
smoking and hearing loss. The purpose of our article was to evaluate the association
between cigarette smoking and hearing loss in a large population-based cohort
of adults aged 48 to 92 years.
A private census was conducted between September 15, 1987, and May 4,
1988, to identify residents of the city or township of Beaver Dam, Wis, who
were aged 43 to 84 years.13 This cohort was
subsequently invited to participate in the Beaver Dam Eye Study, a study of
age-related ocular disorders.14,15
Of the 5924 eligible people, 4926 (83%) participated in the eye examination
phase (1988-1990). Participants of this study who were alive as of March 1,
1993, were eligible for the Epidemiology of Hearing Loss Study (n=4541), which
occurred at the time of the 5-year follow-up visit for the eye study. Of those
eligible, 3753 (82.6%) participated in the hearing study, 180 (4.0%) died
prior to being seen, 604 (13.3%) refused to participate, and 4 (0.1%) were
lost to follow-up. Some participants (n = 182) completed the interview but
refused the hearing test. These participants were excluded from analyses.
The average age of participants was 65.8 years, and 57.7% were women.
Comparisons between participants and nonparticipants have been reported previously.16 In brief, nonparticipants were slightly older (by
an average of about 4 years), slightly more likely to be male, and more likely
to have died since the examination phase began.
The hearing examination included an otoscopic evaluation,16
a screening tympanogram17,18 (GSI
37 Autotymp, Lucas GSI Inc, Littleton, Mass), and pure-tone air-conduction
and bone-conduction audiometry.16 Audiometric
testing was conducted according to the guidelines of the American Speech-Language-Hearing
Association19 in sound-treated booths (Industrial
Acoustics Company, New York, NY) using clinical audiometers (Virtual 320,
Virtual Corporation, Seattle, Wash) equipped with TDH-50 earphones (Telephonics
Corp, Farmingdale, NY). Insert earphones (E-A-Rtone 3A, Cabot Safety Corp,
Indianapolis, Ind) and masking were used as necessary. Pure-tone air-conduction
thresholds were obtained for each ear at 250, 500, 1000, 2000, 3000, 4000,
6000, and 8000 Hz. Bone-conduction thresholds were measured at only 2 frequencies
(500 and 4000 Hz) because of time constraints. Participants who were unable
to travel to the clinic site (nursing home residents, homebound participants,
and participants living in remote areas; n = 132) were tested at their place
of residence using a portable audiometer (Beltone 112, Beltone Electronic
Corp, Chicago, Ill).
All audiometers were initially calibrated in accordance with American
National Standards Institute (ANSI) specifications and were recalibrated every
6 months during the study period.20 Ambient
noise levels were measured at each home or nursing home visit and were routinely
monitored at the clinic site at the Beaver Dam Community Hospital to ensure
that testing conditions complied with ANSI specifications.21
A questionnaire about ear and hearing-related medical history; noise
exposure during leisure, military service, and work; and self-perceived hearing
function was administered as an interview. Questionnaire data on medical history,
lifestyle factors, and medication use were obtained as part of the 5-year
follow-up examination for the Beaver Dam Eye Study (1993-1995), except for
19 people who participated in the hearing study but refused to participate
in this eye examination. In these cases, the medical history and lifestyle
factors interview was conducted during the hearing examination. Overall, the
average time between the 5-year follow-up eye examination and the baseline
hearing examination was 4.5 days. Cigarette smoking status at the time of
the baseline hearing examination in 1993 through 1995 was determined by self-report.
Participants were classified as either nonsmokers (ie, smoked fewer than 100
cigarettes in their lifetime), ex-smokers, or current smokers. Total pack-years
smoked was defined as the number of cigarettes smoked per day divided by 20
cigarettes per pack, then multiplied by the number of years of smoking. No
questions were asked about exposure to environmental tobacco smoke. As a surrogate
for environmental tobacco smoke exposure in the home, nonsmoking participants
were considered to be exposed if they lived in a 2-person household in which
the other person was a study participant and a current smoker. Nonsmoking
participants who lived either alone or in a 2-person household in which the
other person was a study participant and a nonsmoker or an ex-smoker were
considered unexposed. We did not have information on smoking habits for household
members who were not study participants. This marker may misclassify participants
exposed to tobacco smoke in other settings (eg, work or social settings) and
those who have had past exposure in the home (eg, lived with a smoker in the
past) as unexposed.
A history of cardiovascular disease was considered to be present if
the person reported having had a stroke, myocardial infarction, or angina.
Alcohol consumption was measured by a quantity and frequency questionnaire
and converted to grams of ethanol per week. History of occupational noise
exposure was considered positive if the person reported ever having a job
where he or she had to speak in a raised voice to be heard; being a farmer
and driving a tractor without a cab; or having military service with noise
exposure (pilot; airplane or tank crew member; worked in the engine room of
a ship; or used grenades, mortars, shoulder-held grenade launchers, or weapons
systems requiring more than 1 person for operation).
For the purposes of this article, hearing loss was defined as a pure-tone
average (PTA) of thresholds at 500, 1000, 2000, and 4000 Hz greater than 25-dB
hearing level (dB HL) in the worse ear. The worse ear was chosen in order
to include people with at least 1 affected ear. Severity of hearing loss was
classified as mild (>25-dB HL and ≤40-dB HL), moderate (>40-dB HL and ≤60-dB
HL), or marked (>60-dB HL) based on this pure-tone average.
Participants who reported having a hearing loss at younger than 30 years
or a history of ear surgery or whose examination data showed unilateral hearing
loss or hearing loss with a conductive component (air-bone gap ≥15-dB HL
at 500 and/or 4000 Hz) that, if treated and resolved, would leave them with
normal hearing thresholds (PTA <25-dB HL in both ears based on bone conduction)
were considered to have a hearing loss that was not consistent with presbycusis.
A unilateral loss was defined as one ear having a PTA of greater than 25-dB
HL, the opposite ear having a PTA of 25-dB HL or less, and a 20-dB or greater
difference in PTA between ears.
Analyses were conducted using SAS Version 6.09 software (SAS Institute
Inc, Cary, NC). Univariate analyses used the χ2 test of association
for categorical variables, the Mantel-Haenszel test of trend22
for ordinal data, and Student t tests of differences
in means for continuous data. Logistic regression was used to evaluate the
odds of having a hearing loss associated with smoking adjusting for age, sex,
and other potential confounders.23 Interaction
effects of age group and smoking and gender and smoking were tested but eliminated
from the presented models as they were not statistically significant.
Table 1 presents the descriptive
characteristics of participants in the study. Overall, 45.9% had a mild or
greater hearing loss. Forty-six percent of participants were nonsmokers, 39.3%
were ex-smokers, and 14.7% were current smokers. The number of pack-years
of smoking ranged from 0 to 250, with an average of 34.9 pack-years among
current smokers and 28.2 pack-years among ex-smokers. Current smokers reported
smoking an average of 17.5 cigarettes per day (SD, 9.9). Smoking patterns
varied greatly by age, with few older people reporting being current smokers
In age-specific analyses, smoking history was associated with hearing
loss in all but the oldest age group (Table
2). In each age group, the prevalence of hearing loss was higher
among current smokers than nonsmokers.
After adjusting for age, history of cardiovascular disease, alcohol
consumption, occupational noise exposure, and education in a logistic regression
model, current smokers had an increased risk of having a hearing loss compared
with nonsmokers (odds ratio [OR], 1.69; 95% confidence interval [CI], 1.31-2.17)
Prevalent hearing loss in a cohort of older people may be caused by
reasons other than presbycusis. For example, the hearing loss may have developed
at a young age or may represent noise-induced hearing loss. This heterogeneity
may lead to spurious associations or may make it more difficult to detect
an association. To address these concerns, we conducted 2 sets of analyses
to evaluate the consistency of this association in subgroups more likely to
We evaluated the association between smoking and hearing loss in participants
with (n=1903) and without (n= 1536) a history of occupational noise exposure
because people with a history of occupational noise exposure may have noise-induced
hearing loss rather than presbycusis (Table
3). The smoking and hearing loss relationship remained statistically
significant in participants with a history of occupational noise exposure
(OR, 1.85; 95% CI, 1.33-2.57) and those without occupational noise exposure
(OR, 1.53; 95% CI, 1.03-2.29) after controlling for age, sex, history of cardiovascular
disease, alcohol consumption, and education.
We excluded from the analyses participants with hearing loss that was
inconsistent with presbycusis (ie, onset of hearing loss at <30 years,
a history of ear surgery, a conductive hearing loss without any evidence of
decreased hearing sensitivity if the conductive loss were resolved, or a unilateral
hearing loss) (n=269). Current smokers, as shown in Table 3, continued to be more likely to have a hearing loss than
nonsmokers (OR, 1.95; 95% CI, 1.48-2.57) after adjusting for age, sex, history
of cardiovascular disease, alcohol consumption, history of occupational noise
exposure, and education.
The association between pack-years of exposure and hearing loss was
evaluated to determine if risk of hearing loss varied by amount of exposure.
As shown in Table 4, in age-specific
analyses, pack-years of smoking were associated with the prevalence of hearing
loss in all but the oldest age group (P for trend
<.001). After adjusting for age, sex, cardiovascular disease, education,
alcohol consumption, and occupational noise exposure, pack-years of smoking
remained significantly associated with hearing loss (P=.02).
Those in the highest exposure category (≥40 pack-years) were 1.30 times
as likely to have a hearing loss as those with 0 pack-years of exposure (95%
To test for a dose-response relationship among those exposed to cigarette
smoking, these analyses were repeated excluding nonsmokers. As shown in Table 4, there was a statistically significant
test of trend for the association between pack-years and hearing loss among
participants aged 60 to 69 years, with a borderline association among those
aged 48 to 59 years and 80 to 92 years. In a logistic regression model adjusted
for age and sex, participants in the highest exposure category were 1.27 times
as likely to have a hearing loss as those with fewer than 10 pack-years of
smoking exposure (95% CI, 0.96-1.69; P=.09).
Among nonsmoking participants, 78.6% reported living alone or living
with a study participant. In this subset (n= 1113), the first nonsmoking participant
was considered the index case (the person of interest in the analysis). If
the nonsmoker lived with a current smoker, the index case was considered to
be exposed to environmental tobacco smoke (n= 53). Nonsmokers who lived alone
or lived with a nonsmoking or ex-smoking study participant were considered
currently unexposed to environmental tobacco smoke (n=1060). In this subset,
those who lived with a household member who smoked were more likely to have
a hearing loss than those who did not live with a smoker (OR, 1.94; 95% CI,
1.01-3.74; P=.047), after adjusting for age, sex,
history of cardiovascular disease, alcohol consumption, education, and occupational
In this large population-based study, participants who were current
cigarette smokers were 1.7 times as likely to have hearing loss as nonsmokers.
This association was statistically significant after adjusting for the potential
confounding effects of age, sex, education, occupational noise exposure, cardiovascular
disease, and alcohol consumption. In age-specific analyses, this pattern was
consistent for all but the oldest age group, which may be because of the small
number of current smokers (n=13) and the effects of selective mortality. The
odds of having a hearing loss increased with pack-years of smoking and were
higher for nonsmokers living with a current smoker. These results are consistent
with early clinical studies reporting decreased hearing sensitivity in smokers
compared with nonsmokers,4-9
animal studies showing cochlear damage after exposure to cigarette smoke,4 and population-based self-reported data from the Health
No association between cigarette smoking and hearing loss was found
in the population-based Framingham Study.12
In that study, analyses focused on low-frequency and high-frequency hearing
separately and a higher cut point (>40-dB HL) was used to classify hearing
loss. These methodological differences may account, in part, for the discrepant
results. For example, people with mild hearing losses and those with sloping
high-frequency hearing losses typical of presbycusis were classified as having
normal hearing in some analyses. This misclassification may have biased the
findings, making it difficult to detect an association with smoking. In addition,
analyses were conducted for men and women separately, decreasing the power
to detect an association in the absence of evidence of a gender-smoking interaction.
In the current study, there was no significant interaction between gender
and smoking (data not shown).
The Baltimore Longitudinal Study of Aging resulted in the only article
(to our knowledge) evaluating the longitudinal association between smoking
and hearing loss. In that study, no association was found between current
(baseline) smoking habits and the incidence of hearing loss.10
However, there were only 46 incident cases of hearing loss among the 531 men
participating in the study, which may have limited the power to detect an
Whereas the current study relies on self-report of smoking behavior,
which may be a biased measure because of underreporting, the association with
number of pack-years of exposure suggests that any misclassification effects
may have biased the results toward the null. There was weak evidence of a
dose-response relationship among smokers after adjusting for age and sex (P=.09). The failure to detect a strong dose-response relationship
may reflect the limitations of the self-reported estimate of lifetime exposure,
the effects of selective mortality, or the impact of cohort effects because
few participants older than 70 years had ever smoked.
The finding of an association with exposure to environmental tobacco
smoke in the home is consistent with reports of effects of passive smoking
on hearing sensitivity in children.24,25
The measure of exposure to environmental tobacco smoke in the home used in
this study may be a poor marker for total exposure. We did not ask questions
about exposure to secondhand smoke in the home, workplace, or in social settings.
Because of the population-based nature of the study, we were able to identify
a subset of nonsmokers who either lived alone or with another study participant
who had provided self-reported smoking behavior. However, participants currently
exposed to significant amounts of environmental tobacco smoke in settings
outside of the home may have been misclassified as unexposed. This crude index
of exposure to environmental tobacco smoke did not include information on
past exposure, intensity of exposure, or duration of exposure. Thus, these
data should be interpreted cautiously. Whereas these biases would tend to
increase the likelihood of failing to detect an association, it is possible
that factors unaccounted for in our analytic model may explain this association.
Studies using quantitative methods for measuring exposure to environmental
tobacco smoke are needed to thoroughly evaluate this relationship. The point
estimate for the association between environmental tobacco smoke exposure
in the home and hearing loss appears to be larger than the estimate for smoking
history. However, because of the broad confidence limits, this should not
be interpreted as suggesting that passive smoking has a greater effect than
Cigarette smoking is well recognized to be associated with other lifestyle
and socioeconomic factors that may adversely affect health. For example, people
who smoke may be more likely to be exposed to noisy workplaces and leisure
activities, they may be more likely to consume alcoholic beverages, and they
may have chronic conditions, such as heart disease, that may be associated
with hearing loss. In models that included alcohol consumption, cardiovascular
disease, education, and occupational noise exposure to adjust for potential
confounding effects, smoking history remained significantly associated with
hearing loss, suggesting that smoking is not merely serving as a marker for
other lifestyle factors. The inclusion of leisure-time noise exposure or the
number of medications used did not alter the results (data not shown).
These data suggest that cigarette smoking, a well-known risk factor
for other chronic diseases, may affect hearing sensitivity. Cigarette smoking
may affect hearing through its effects on antioxidative mechanisms or on the
vasculature supplying the auditory system.4,5
Recently, animal studies have identified nicotinic-like receptors in the hair
cells, which suggests that smoking may have direct ototoxic effects on hair
cell function through its potential effect on the neurotransmission of auditory
In summary, the findings from this cross-sectional, population-based
study are consistent with the literature and suggest that environmental exposures
may play a role in age-related hearing loss. If longitudinal, population-based
studies confirm these findings, modification of smoking habits may prevent
or delay age-related declines in hearing sensitivity.
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